Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endothelin-1 (ET-1) is a potent vasoactive peptide that has been reported to cause lung edema. This study tested if the edemagenic effect of ET-1 is due to preferential venoconstriction and, if so, whether the site of resistance is similar with salt solution (PSS) and more physiologic blood perfusate. ET-1 caused concentration-dependent contraction of pulmonary arterial and venous rings, with an EC50 of 1.3 nM in artery and 0.6 nM in vein (p less than 0.05). In PSS-perfused lungs, 5 nM ET-1 caused a 7.0 +/- 0.8 torr pressor response that was associated with a 5.0 +/- 0.3 torr increase in microvascular pressure and a 530 +/- 20 mg increase in lung weight within 10 min. In contrast, KCl-treated lungs had an equivalent pressor response (7.4 +/- 1.1 torr), yet the microvascular pressure increased by only 2.5 +/- 0.4 torr (p less than 0.05 from ET-1) and the lung weight was unchanged. Meclofenamate did not prevent the effect of ET-1 on microvascular pressure or lung weight. In blood-perfused lungs, ET-1 caused a 7.3 +/- 0.1 torr pressor response but only a 2.0 +/- 0.5 torr increase in microvascular pressure and no increase in lung weight. ET-1 had no effect on permeability either of cultured endothelial cell monolayers or in the pulmonary microvasculature in vivo. We conclude that the edemagenic effect of ET-1 in PSS-perfused lungs is mediated through venoconstriction and an increase in microvascular pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endothelin-1 increases the pulmonary microvascular pressure and causes pulmonary edema in salt solution but not blood-perfused rat lungs. 128 Jul 24

Eight rat lungs were perfused in an in vitro circuit with a blood-PS solution and then with a perfluorocarbon emulsion (perfluorotributylamine, FC-43). With perfusion flow constant, the hypoxic pulmonary vasoconstrictor (HPV) response was measured as changes in pulmonary artery pressure when F1,O2 was changed to 0.1, 0.06, 0.04, 0.03, 0.02 and zero with FI,CO2 of 0.05. The hypoxic response to an FI,O2 of 0.03, with the blood-PSS perfusate, was an increase from baseline pressure of 93.5 +/- 18% and, with the perfluorocarbon perfusate was 67.5 +/- 18%; these values were not significantly different (P greater than 0.2). A stimulus-response relationship was obtained with the FC-43 perfusate by plotting the response as a percentage of the maximum response (R%max) against the logarithm of the alveolar oxygen tension. The equation for the linear portion of the response was R%max = 257.9-140.2 X log (10) PA,O2 and r = 0.78. The PA,O2 corresponding to half of the maximum response (ED50) was 30.4 mmHg. The present study demonstrated that HPV is maintained in isolated rat lungs perfused with an FC-43 emulsion. The stimulus-response relationship as well as the ED50 with the FC-43 is similar to earlier results with blood perfusate. Lung oedema was not found after perfusion with the FC-43 emulsion.
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PMID:Hypoxic pulmonary vasoconstriction in isolated rat lungs perfused with perfluorocarbon emulsion. 406 Nov 15